Role of immune responses in protection and pathogenesis during Semliki Forest virus encephalitis

Amor, Sandra; Scallan, Martina F.; Morris, Michael; Dyson, Heather; Fazakerley, John K.

doi:10.1099/0022-1317-77-2-281

Cited by 90 publications

(76 citation statements)

References 28 publications

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“…21,22 As expected, no neurological deficits or altered behavior could be observed during the experiments in the present study, and the mice remained alert, ate and drank normally and did not lose weight.…”

Section: Presence Of Sfv A7(74) Virus In Nude Mouse Tumors and Brainmentioning

confidence: 50%

“…We did not analyze the tissues beyond 1 week p.i., but it is likely that the virus is cleared and becomes undetectable by immunohistochemistry at later time points. Namely, other groups have reported a transient decline in CNS virus titers in infected nude mice, 22,24 although viral RNA could still be detected by in situ hybridization. The decline in virus antigen observed in the present study correlates with peaking of virus-specific IgM and the leakiness of the bloodbrain-barrier that occurs during infection with avirulent SFV.…”

Section: Discussionmentioning

confidence: 99%

“…We expected no side effects in the present study as SFV A7 (74) is avirulent in both normal immunocompetent animals as well as in nude mice. 21,22 On the other hand, it was not clear whether the immune system would allow the virus enough time to successfully find and destroy the tumors.…”

Section: Discussionmentioning

confidence: 99%

“…Although not analyzed in the present study, the A7(74) CNS titers have been shown to be restricted also in nude and SCID mice (several magnitudes lower than in WT SFV), indicating that the restriction of A7(74) replication is not mediated by cells of the adaptive immune system. 22,24 The efficacy of the virotherapy in the nude mouse model is demonstrated in Figure 1. However, as opposed to the SCID mouse tumor model data in our previous study, 15 only the intratumoral administration route was effective.…”

Section: Discussionmentioning

confidence: 99%

“…The decline in virus antigen observed in the present study correlates with peaking of virus-specific IgM and the leakiness of the bloodbrain-barrier that occurs during infection with avirulent SFV. 21,22,[24][25][26] We therefore believe that virus-specific IgM may have inhibited virus replication below the detection limit due to temporary access of serum components to the CNS. Although not analyzed in the present study, the A7(74) CNS titers have been shown to be restricted also in nude and SCID mice (several magnitudes lower than in WT SFV), indicating that the restriction of A7(74) replication is not mediated by cells of the adaptive immune system.…”

Section: Discussionmentioning

confidence: 99%

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Evaluation of cancer virotherapy with attenuated replicative Semliki forest virus in different rodent tumor models

Määttä

Liimatainen

Wahlfors

et al. 2007

Intl Journal of Cancer

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Semliki Forest virus (SFV) is one of the latest candidates for a virotherapeutic agent against cancer, and recent studies have demonstrated its efficacy in tumor models. In the present study, we examined the antitumor efficacy of an avirulent SFV strain A7(74) and its derivative, a replication-competent SFV vector VA7-EGFP, in a partially immunodeficient mouse tumor model (subcutaneous A549 human lung adenocarcinoma in NMRI nu/nu mouse) and in an immunocompetent rat tumor model (intracranial BT4C glioma in BDIX rat). When subcutaneous mouse tumors were injected 3 times with VA7-EGFP, intratumorally treated animals showed almost complete inhibition of tumor growth, while systemically treated mice displayed only delayed tumor growth (intravenous injection) or no response at all (intraperitoneal injection). This was at least partially due to a strong type I interferon (IFN) response in the tumors. The animals did not display any signs of abnormal behavior or encephalitis, even though SFV-positive foci were detected in the brain after the initial blood viremia. Intracranial rat tumors were injected directly with SFV A7(74) virus and monitored with magnetic resonance imaging. Tumor growth was significantly reduced (p < 0.05) with one virus injection, but the tumor size continued to increase after a lag period and none of the treated animals survived. Three virus injections or T-cell suppression with dexamethasone did not significantly improve treatment efficacy. It appeared that the local virotherapy induced extensive production of neutralizing anti-SFV antibodies that most likely contributed to the insufficient treatment efficacy. In conclusion, we show here that SFV A7(74) is a potential oncolytic agent for cancer virotherapy, but major immunological hurdles may need to be overcome before the virus can be clinically tested. ' 2007 Wiley-Liss, Inc.

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Section: Presence Of Sfv A7(74) Virus In Nude Mouse Tumors and Brainmentioning

confidence: 50%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 3 more Smart Citations

Evaluation of cancer virotherapy with attenuated replicative Semliki forest virus in different rodent tumor models

Määttä

Liimatainen

Wahlfors

et al. 2007

Intl Journal of Cancer

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Transient virus infection and multiple sclerosis

Atkins

McQuaid²,

Morris-Downes

et al. 2000

Rev. Med. Virol.

Self Cite

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Biological models in multiple sclerosis

Sanabria-Castro

Flores-Dı́az

Alape-Girón

2019

J of Neuroscience Research

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Considering the etiology of multiple sclerosis (MS) is still unknown, experimental models resembling specific aspects of this immune‐mediated demyelinating human disease have been developed to increase the understanding of processes related to pathogenesis, disease evolution, evaluation of therapeutic interventions, and demyelination and remyelination mechanisms. Based on the nature of the investigation, biological models may include in vitro, in vivo, and ex vivo assessments. Even though these approaches have disclosed valuable information, every disease animal model has limitations and can only replicate specific features of MS. In vitro and ex vivo models generally do not reflect what occurs in the organism, and in vivo animal models are more likely used; nevertheless, they are able to reproduce only certain stages of the disease. In vivo MS disease animal models in mammals include: experimental autoimmune encephalomyelitis, viral encephalomyelitis, and induced demyelination. This review examines and describes the most common biological disease animal models for the study of MS, their specific characteristics and limitations.

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Role of immune responses in protection and pathogenesis during Semliki Forest virus encephalitis

Cited by 90 publications

References 28 publications

Evaluation of cancer virotherapy with attenuated replicative Semliki forest virus in different rodent tumor models

Evaluation of cancer virotherapy with attenuated replicative Semliki forest virus in different rodent tumor models

Transient virus infection and multiple sclerosis

Biological models in multiple sclerosis

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